RNAseq analysis of skeletal muscle transcriptomes from wild-type, FNIP1-knockout (FNIP1-KO) mice, and mice expressing FNIP1 only in skeletal muscle (FNIP1-TgKO).
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ABSTRACT:
PROVIDER: PRJNA631493 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11745686_1.fastq.gz | Fastqsanger.gz | |||
| SRR11745686_2.fastq.gz | Fastqsanger.gz | |||
| SRR11745687_1.fastq.gz | Fastqsanger.gz | |||
| SRR11745687_2.fastq.gz | Fastqsanger.gz | |||
| SRR11745688_1.fastq.gz | Fastqsanger.gz |
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Project description:This experiment was conducted to identify FNIP1-dependent mRNA transcripts alteration in skeletal muscle. Mouse FNIP1 was specifically overexpressed in skeletal muscle in FNIP1-transgenic (FNIP1-Tg) mice. FNIP1-Tg mice were crossed with FNIP1-knockout (FNIP1-KO) mice to generate FNIP1-TgKO mice expressing FNIP1 only in skeletal muscle but not in other tissues. The muscle glycolytic-to-oxidative transformation is determined, largely in part, at the level of gene expression. To gain insight into the FNIP1-dependent regulation of skeletal muscle energy metabolism, transcriptome analysis was performed by whole-genome gene expression profiling experiments in gastrocnemius (GC) muscle from both FNIP1-KO and FNIP1-TGKO mice. We were particularly interested in the subset of genes that were regulated only in the FNIP1-KO mice but not in FNIP1-TGKO mice. Gene ontology (GO) analysis revealed that the primary FNIP1-regulated genes were mitochondrial metabolic genes. A broad array of genes involved in mitochondria was regulated FNIP1-KO muscle in a FNIP1-dependent manner. Together, the transcriptional profiling results indicate that a significant subset of FNIP1 target genes, were those involved in mitochondrial function.
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Project description:This experiment was conducted to identify target genes of the microRNA-499 in skeletal muscle of transgenic mice that overexpressed miR-499. The following abstract from the submitted manuscript describes the major findings of this work. Coupling of mitochondrial function and skeletal muscle fiber type by a miR-499/Fnip1/AMPK circuit. Jing Liu, Xijun Liang, Danxia Zhou, Ling Lai, Tingting Fu, Yan Kong, Qian Zhou, Rick B. Vega, Min-Sheng Zhu, Daniel P. Kelly, Xiang Gao, and Zhenji Gan. Upon adaption of skeletal muscle to physiological and pathophysiological stimuli, muscle fiber type and mitochondrial function are coordinately regulated. Recent studies have identified pathways involved in control of contractile proteins of oxidative type fibers. However, the mechanism for coupling of mitochondrial function to muscle contractile machinery during fiber type transition remains unknown. Here, we show that the expression of the genes encoding type I myosins, Myh7/Myh7b and their intronic miR-208b/miR-499 parallels mitochondrial function during fiber type transitions. Using in vivo approaches in mice, we found that miR-499 drives a PGC-1a-dependent mitochondrial oxidative metabolism program to match shifts in slow-twitch muscle fiber composition. Mechanistically, miR-499 directly targets Fnip1, a known AMP-activated protein kinase (AMPK)-interacting protein that negatively regulates AMPK, a known activator of PGC-1a. Inhibition of Fnip1 reactivated AMPK/PGC-1a signaling and mitochondrial function in myocytes. Restoration of the expression of miR-499 in the mdx mouse model of Duchenne muscular dystrophy (DMD) reduced the severity of DMD. Thus, we have identified a miR-499/Fnip1/AMPK circuit that can serve as a mechanism to couple muscle fiber type and mitochondrial function. Keywords: muscle, contractile fiber type, mitochondrial function, microRNA, gene regulation RNA from three wild-type (non-transgenic (NTG)) and three miR-499 overexpressing (MCK-miR-499) mice was analyzed. three replicates of each are provided.
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Project description:This experiment was conducted to identify target genes of the microRNA-499 in skeletal muscle of transgenic mice that overexpressed miR-499. The following abstract from the submitted manuscript describes the major findings of this work. Coupling of mitochondrial function and skeletal muscle fiber type by a miR-499/Fnip1/AMPK circuit. Jing Liu, Xijun Liang, Danxia Zhou, Ling Lai, Tingting Fu, Yan Kong, Qian Zhou, Rick B. Vega, Min-Sheng Zhu, Daniel P. Kelly, Xiang Gao, and Zhenji Gan. Upon adaption of skeletal muscle to physiological and pathophysiological stimuli, muscle fiber type and mitochondrial function are coordinately regulated. Recent studies have identified pathways involved in control of contractile proteins of oxidative type fibers. However, the mechanism for coupling of mitochondrial function to muscle contractile machinery during fiber type transition remains unknown. Here, we show that the expression of the genes encoding type I myosins, Myh7/Myh7b and their intronic miR-208b/miR-499 parallels mitochondrial function during fiber type transitions. Using in vivo approaches in mice, we found that miR-499 drives a PGC-1a-dependent mitochondrial oxidative metabolism program to match shifts in slow-twitch muscle fiber composition. Mechanistically, miR-499 directly targets Fnip1, a known AMP-activated protein kinase (AMPK)-interacting protein that negatively regulates AMPK, a known activator of PGC-1a. Inhibition of Fnip1 reactivated AMPK/PGC-1a signaling and mitochondrial function in myocytes. Restoration of the expression of miR-499 in the mdx mouse model of Duchenne muscular dystrophy (DMD) reduced the severity of DMD. Thus, we have identified a miR-499/Fnip1/AMPK circuit that can serve as a mechanism to couple muscle fiber type and mitochondrial function. Keywords: muscle, contractile fiber type, mitochondrial function, microRNA, gene regulation
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